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1 Pathology Week 13: the Lung Ver.2

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1 Pathology Week 13: the Lung Ver.2 Pathology week 13: the Lung ver.2 Atelectasis - either incomplete expansion of the lungs (neonatal) or collapse of previously inflated lung, producing areas of relatively airless pulmonary parenchyma - reduces oxygenation, predisposes to infection - reversible except if caused by contraction o acquired either: resorption atelectasis (obstruction airway, resorption trapped oxygen) • mucus plugging eg asthma, bronchitis, bronchiectasis, post op, FBs • mediastinum shifts towards affected lung compression atelectasis • effusion, pneumothorax, haemothorax, peritonitis – basal atelectasis • mediastinum shift away from affected lung contraction atelectasis • when local or general fibrotic changes in lung prevent full expansion Acute Lung Injury - a spectrum of pulmonary lesions (endothelial and epithelial) - initiated by many factors - susceptibility my be heritable - mediators include cytokines, oxidants, growth factors (incl TNF, IL1, IL6, IL10, TGFβ) - may manifest as congestion, oedema, surfactant disruption, atelectasis - may progress to ARDS or acute interstitial pneumonia Pulmonary Oedema - most common haemodynamic mechanism: ↑ hydrostatic pressure in LVF - heavy, wet lungs – initially basal due to greater hydrostatic pressure - alveolar capillaries engorged, intra-alveolar granular pink precipitate, alveolar microhaemorrhages and haemosiderin-laden macrophages (“heart failure” cells ) - longstanding LVF – many haemosiderin-laden macrophages, fibrosis, thickening alveolar walls – lungs firm and brown (brown induration) Oedema caused by microvascular injury - injury to capillaries of alveolar septa - usually normal hydrostatic pressure - oedema due to primary injury to vascular endothelium or damage to alveolar epithelial cells, with secondary microvascular injury - results in leakage of fluids and proteins into interstitial space, and if severe also into alveoli - can be localised (as in pneumonia) or diffuse (contributing to ARDS) Classification/causes pulmonary oedema Haemodynamic oedema ↑ hydrostatic pressure (↑ pulm venous pressure) - LVF (common) - volume overload - pulm vein obstruction ↓ oncotic pressure (less common) - hypoalbuminaemia - nephritic syndrome - liver disease - protein-losing enteropathies lymphatic obstruction (rare) Oedema due to microvascular injury (alveolar injury) - infections (pneumonia, septicaemia) - inhaled gases (oxygen, smoke) - liquid aspiration (gastric contents, near-drowning) - drugs and chemicals (chemo – bleomycin, amphotericin B, heroin, kerosene, paraquat) - shock, trauma - radiation - transfusion related 1 Oedema of undetermined origin - high altitude - neurogenic (CNS trauma) Acute respiratory distress syndrome (diffuse alveolar damage) - caused by diffuse alveolar capillary damage (DAD) - rapid onset life threatening respiratory insufficiency, cyanosis and severe arterial hypoxaemia refractory to oxygen therapy, may progress to multiorgan failure - complication of may conditions, often a combination of predisposing factors (eg shock, O2 therapy, sepsis) Conditions associated with development of ARDS Infection - sepsis, diffuse pulmonary infections (viral, mycoplasma, PCP, military TB), aspiration Physical injury - trauma incl head injuries, pulmonary contusion, near-drowning, fat emboli with fractures, burns, ionizing radiation Inhaled irritants - oxygen toxicity, smoke, irritant gases/chemicals Chemical injury - overdose heroin, methadone, aspirin, barbiturate, paraquat Haematological conditions - multiple transfusions, DIC Pancreatitis Uraemia Cardiopulmonary bypass Hypersensitivity reactions (>50% cases due to sepsis, pulmonary infections, aspiration or head injuries) Pathogenesis ARDS - central to causation: diffuse damage to alveolar capillary walls, with a number of steps leading to resp failure - cf. respiratory distress of newborns due to lack of surfactant 1. result of cascade of cellular events initiated by infectious or non-infectious inflammatory stimuli 2. initial injury to either capillary endothelium (most frequently) or alveolar epithelium 3. as early as 30 minutes following acute insult (e.g., acid aspiration, trauma, exposure to bacterial LPS), ↑ synthesis IL-8 by pulmonary macrophages (potent neutrophil chemotactic and activating agent) 4. along with other cytokines eg IL1 and TNF, leads to pulmonary microvascular sequestration of neutrophils then margination into alveolar space where they are activated 5. activated neutrophils release variety of products incl oxidants, proteases, platelet-activating factor, and leukotrienes that cause active tissue damage 6. cause ↑ vascular permeability and alveolar oedema, loss of diffusion capacity, and surfactant inactivation caused by damage to type II pneumocytes, and hyaline membrane formation 7. release of macrophage inhibitory factor (MIF) sustains the ongoing inflammatory response 8. release of macrophage-derived fibrogenic cytokines such as transforming growth factor β (TGF-β) and platelet-derived growth factor (PDGF) stimulate fibroblast growth and collagen deposition associated with the healing phase of injury 2 Morphology ARDS - acutely lungs heavy, red, firm, boggy. Congestion, interstitial and intra-alveolar oedema, inflammation, fibrin deposits. Alveolar walls lined with waxy hyaline membrane - organising stage: type II epithelial cells proliferate to regenerate alveolar lining. Organisation and fibrosis of exudate – resolution unusual. +/- superimposed infection Clinical course ARDS - marked dyspnoea and tachypnoea but CXR initially normal - ↑ cyanosis, hypoxemia, respiratory failure, appearance diffuse bilateral infiltrates on CXR. - hypoxemia can become unresponsive to oxygen therapy, respiratory acidosis can develop Poorly aerated regions still perfused, so V-Q mismatch and hypoxemia. Mortality ~60%. Acute Interstitial Pneumonia - clinicopathologic term used to describe widespread acute lung injury with a rapidly progressive clinical course similar to that seen in ARDS - ARDS associated with known causes eg sepsis, pulmonary infection, gastric aspiration, and trauma, acute interstitial pneumonia is of unknown aetiology - present with acute respiratory failure often following <3/52 URTI-like illness ; mortality rate ~ 50% Obstructive vs Restrictive Lung Diseases 2 categories diffuse pulmonary disease: (1) obstructive (or airway disease): ↑ resistance to airflow due to partial or complete obstruction - PFTs show limitation max airflow rates during forced expiration (measured FEV1) - exp flow obstruction due to airway narrowing (asthma), or loss elastic recoil (emphysema) - emphysema, chronic bronchitis, bronchiectasis, asthma (2) restrictive ↓ expansion lung parenchyma, with ↓ TLC - normal or proportionately ↓ flow rate - 1. chest wall disorders with normal lungs (e.g., neuromuscular diseases -polio, severe obesity, pleural diseases, kyphoscoliosis) - 2. acute or chronic interstitial and infiltrative diseases. (acute – ARDS; chronic - pneumoconioses, interstitial fibrosis of unknown aetiology, and most infiltrative conditions) Obstructive Pulmonary Diseases - emphysema, chronic bronchitis, asthma, bronchiectasis → common trigger (smoking) Emphysema abnormal permanent enlargement airspaces distal to terminal bronchiole, with destruction of walls and without fibrosis Disorders Associated with Airflow Obstruction Anatomic Clinical Term Site Major Pathologic Changes Aetiology Signs/Symptoms Chronic bronchitis Bronchus Mucous gland hyperplasia, Smoking, pollution Cough, sputum hypersecretion production Bronchiectasis Bronchus Airway dilation and scarring Persistent or severe Cough, purulent infections sputum, fever Asthma Bronchus Smooth muscle hyperplasia, Immunologic or Episodic wheezing, excess mucus, inflammation undefined causes cough, dyspnoea Emphysema Acinus Airspace enlarge; wall Smoking Dyspnoea destruction Small airway disease, Bronchiole Inflam scarring/obliteration Smoking, pollution, Cough, dyspnoea bronchiolitis miscellaneous Types of Emphysema Classified according to anatomic distribution within the lobule (cluster of acini). (1) centriacinar (centrilobular) – 95% cases (2) panacinar (3) paraseptal (distal acinar) (4) irregular 3 Centriacinar (centrilobular) Emphysema - central or proximal parts of acini, formed by respiratory bronchioles affected, distal alveoli spared - more common and more severe in upper lobes - walls of emphysematous spaces often contain large amounts of black pigment - inflammation around bronchi and bronchioles is common - in severe centriacinar emphysema, the distal acinus may be involved - predominantly in heavy smokers, often in association with chronic bronchitis Panacinar (panlobular) Emphysema - acini uniformly enlarged from respiratory bronchiole to terminal blind alveoli - occur more commonly in the lower zones and anterior margins of the lung - associated with α 1-antitrypsin (α 1-AT) deficiency Distal Acinar (Paraseptal) Emphysema - proximal portion of acinus normal, but distal part is predominantly involved - more severe in upper half of lungs - multiple, continuous, enlarged airspaces from less than 0.5 cm to more than 2.0 cm in diameter, sometimes forming cystlike structures - probably underlies many cases of spontaneous pneumothorax in young adults Airspace Enlargement with Fibrosis (Irregular Emphysema) - associated with scarring - most common form of emphysema because most lungs at autopsy shows one or more scars from a healed inflammatory process - these foci of irregular emphysema are asymptomatic Incidence - fourth leading cause of morbidity and mortality
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